Gastro-esophageal reflux disease is a widespread affliction, which frequently elevates to be a clinical problem for the patient. It has been suggested that about ten percent of the U.S. population may have what is referred to as daily heartburn, and that more than one-third of the population has intermittent symptoms. See "Guidelines for the Diagnosis and Treatment of Gastro-Esophageal Reflux Disease," Arch Intern Med., Fall, 155, Nov. 13, 1995. Most therapies for GERD, which has a number of different manifestations, have historically been directed at neutralization or suppression of gastric acid. Although the use of antacid for self-medication of symptoms of GERD is prodigious, unfortunately many patients with mild esophagitis nonetheless progress to a more severe form of the disease.
While it is commonly said that the underlying problem that produces GERD is abnormal acid secretion, the literature suggests that in fact it is largely an esophageal motility disorder. See "Guidelines for the Diagnosis and Treatment of Gastro-Esophageal Reflux Disease," DeVault and Castell, Arch. Intern. Med., Vol. 155, Nov. 13, 1995, pp.2165-2173. By this it is meant that GERD is caused by abnormal motility which allows a breakdown of the anti-reflux barriers provided by the lower esophageal sphincter (LES) and esophageal-clearing peristalsis. The data point to decreased LES pressures in reflux patients. The more severe cases appear to be in patients having lower LES pressures with lower peristaltic amplitudes and abnormal peristalsis.
It is not clear whether the poor motility and low esophageal pressures of GERD patients precede esophageal mucosal reflux damage, or whether repeated reflux first results in a progressive decline in LES pressure. In any event, most patients with GERD who exhibit substantial esophageal injury also have abnormal LES pressures. One illustrative attempt to treat GERD with stimulation is shown in U.S. Pat. No. 5,716,385, Mittal et al. In that system, the skeletal muscles of the crural diaphragm are stimulated during relaxations of the diaphragm, causing contraction of the LES. However, this is a very indirect approach; the LES is not directly stimulated. Furthermore, the stimulation is applied only during sensed periods of transient relaxation.
By contrast, it is a premise of the system and method of this invention that therapy for GERD is best provided by substantially continuously increasing LES pressure. It is thus my concept to provide stimulation of the lower esophageal sphincter muscle to produce sustained and continuous contraction of the muscle so as to reduce acid reflux from the stomach. In other words, stimulation of the LES causes it to remain "tonal" or "excited," so that it is "closed" to a sufficient degree to reduce acid reflux from the stomach whenever there may be significant output of gastric acid. The induced constriction of the lower esophageal sphincter by application of stimulus pulses to excite the sphincter muscle will reduce, and indeed can stop ongoing acid damage within the esophagus. By thus correcting the GERD condition, the patient will be relieved from having to rely on costly drugs or surgical procedures, neither of which are reliably effective. Such an implantable system can be used to continuously correct the problem of lower LES pressure. The system can therefore provide a reduction in the number of medical problems, e.g., esophagitis (inflammation of the lower esophagus); bleeding from the lower esophagus due to ulcerations caused by acid reflux; reducing the risk of stricture formation of the lower esophagus from acid injury; and formation of scar tissue due to natural bodily attempts to heal the damaged area. Further, reduction of reflux injury can lower the incidence of cancer of the lower esophagus. In patients who are at increased risk due to Barrett's esophagus, reduction of acid reflux is likely also to reduce the risk of subsequent cancer.